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Coffee and Myocardial Infarction

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To the Editor:

The role of daily activities and events in triggering myocardial infarction (MI) remains inconclusive. Baylin et al1 conducted a study supporting the idea that coffee intake may trigger MI. However, they recognized the possibility of temporal confounding by other external triggers such as smoking, physical, or sexual activity. Additional confounders may be emotional or meteorological stresses,2 but the greatest confounding could be through intake of various substances other than coffee, possibly taken at the same time as the coffee. Food ingestion precedes approximately 8% of MIs2 and has been verified as a trigger of acute coronary syndrome by case–crossover methodology.3 Cold drinks4 and alcoholic drinks5,6 have also been suggested as triggers of sudden cardiac events. Finally, urination and defecation can follow coffee consumption and have been implicated in the triggering of MI.7

Similar to the present study,1Šelb Šemerl and Šelb estimated the hazard period for a cardiac event as 1 hour after ingesting coffee.5 In their study, regular physical activity was not protective, but rather increased the likelihood of sudden cardiac death. It may be that coffee intake predisposes to fatal cardiac arrhythmias in people who are susceptible but apparently healthy (engaging in regular physical activity), whereas in those with a higher risk profile (who have presumably already developed atherosclerosis), coffee may instead trigger typical coronary atherothrombosis.

This is a continuing controversy in the present study.1 The risk of MI was greater among those with 3 or more risk factors for coronary disease; however, when the risk factors were examined separately, the risk of MI was lower among those with hypertension, hypercholesterolemia, or history of previous angina compared with those not having these risk factors.1 Recently, it has been reported that coffee intake increases the risk of nonfatal MI only among individuals with “slow” caffeine metabolism, such as carriers of the variant cytochrome P450 1A2*1F, but not among “rapid” caffeine metabolizers who are homozygous for the cytochrome P450 1A2*1A allele.8 An acute cardiac event is often multifactorial, and the potential of coffee to trigger a specific event should be further defined in relation to an individual’s demographic and risk factor characteristics. A possibility of diverse susceptibility to a particular external trigger according to such characteristics has previously been suggested.2,9

The study by Baylin and colleagues1 corroborates earlier findings10 that people with light or occasional coffee intake may be at higher risk of MI than those with higher intake. Baylin et al reasonably proposed that the triggering effect of coffee could be greater in the morning due to lower plasma caffeine even in heavy drinkers. Moreover, given the fact that coffee is more often used in the morning, these 2 correlated effects may contribute to the morning peak in incidence of MI. Coffee may also contribute to the slight Monday excess in MIs and other acute cardiac events.11 It had been proposed that this excess is an artifact of events with uncertain dates being coded as taking place on Mondays,12 but this has not been supported by more recent meta-analysis.11 In addition to other putative explanations,13 the start of the work week may be accompanied by a relative excess in coffee intake after 2 days of weekend decrease in consumption and tolerance, which could cause a more marked coffee-related sympathetic surge. This sounds more plausible than a Monday excess related to alcohol ingestion,11 since peak consumption of alcohol takes place on Friday and Saturday.13 However, this needs further exploration.

13. Čulić V. Excess in cardiovascular events on Mondays: could atherosclerotic plaques be more vulnerable after the weekend because of alcohol related cytokine dysregulation? J Epidemiol Community Health. 2005;59:911.

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